The Role of Prokineticins in the Pathogenesis of Hypogonadotropic Hypogonadism

被引：29

作者：

Abreu, Ana Paula ^{[2
,3
]}

Kaiser, Ursula B. ^{[2
,3
]}

Latronico, Ana Claudia ^{[1
]}

机构：

[1] Univ Sao Paulo, Lab Hormonios & Genet Mol, Disciplina Endocrinol & Metabol,Hosp Clin, Unidade Endocrinol Desenvolvimento,Fac Med, BR-05403900 Sao Paulo, Brazil

[2] Brigham & Womens Hosp, Div Endocrinol Diabet & Hypertens, Boston, MA 02115 USA

[3] Harvard Univ, Sch Med, Boston, MA USA

来源：

NEUROENDOCRINOLOGY | 2010年 / 91卷 / 04期

基金：

巴西圣保罗研究基金会;

关键词：

Prokineticins; GnRH secretion; Kallmann syndrome; Hypogonadotropic hypogonadism; GONADOTROPIN-RELEASING-HORMONE; KALLMANN-SYNDROME; BIALLELIC MUTATIONS; OLFACTORY-BULB; MICE LACKING; IDENTIFICATION; PROTEIN; GENE; DEFICIENCY; EXPRESSION;

D O I：

10.1159/000308880

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The prokineticin system comprises two multifunctional secreted proteins, prokineticin-1 (PROK1) and prokineticin-2 (PROK2), and their cognate G protein-coupled receptors. The prokineticins were originally identified as endogenous regulators of gastrointestinal motility. Currently, these bioactive peptides are involved in a wide spectrum of biological functions, including angiogenesis, neurogenesis, circadian rhythms, nociception, hematopoiesis and immune response. Mice homozygous for null mutations in Prokr2 or Prok2 recapitulate the human phenotype of Kallmann syndrome, exhibiting severe atrophy of the reproductive system and hypoplastic olfactory bulbs. Indeed, the evidence from several naturally inactivating mutations in the PROK2 and PROKR2 genes in patients with Kallmann syndrome and normosmic hypogonadotropic hypogonadism also indicate the essential role of PROK2 in olfactory bulb morphogenesis and GnRH secretion in humans. Copyright (c) 2010 S. Karger AG, Basel

引用

页码：283 / 290

页数：8

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